Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A representative sample of 117 patients with definite multiple sclerosis (MS) was interviewed on pain syndromes. Chronic syndromes lasting more than one month included dysaestesthesia, low back pain, spasms, tonic seizures, tightening and painful sensations in the extremities. Acute syndromes included neuralgia, L'Hermitte's sign and pain associated with optic neuritis. Thirty-five per cent were pain-free. Of the remaining patients had 45% pain at the time of the examination, 32% indicated pain among the most severe symptoms of MS and 23% had pain at the onset of MS. The number of patients with pain at the time of the examination increased with age and duration of disease. Patients with pain were significantly more often spastic and significantly more often sought alternative treatment forms. No difference was found for mean age, sex, physical impairment, duration of disease from onset of MS, depressive score and score of delayed verbal memory.
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PMID:Acute and chronic pain syndromes in multiple sclerosis. 195 Apr 60

The mean latency and waveform of early and late SEPs recorded on 50 and 200 ms were studied in 20 normal subjects, for the parietal (P), prerolandic (F) and prefrontal (pF) regions, ipsiand contralateral to the stimulated median nerve, using either the midfrontal or ear lobe electrode as reference. N17 (thalamic) potential occurred in the ipsilateral P and both F and pF regions (when using an ear lobe reference). The study was also performed in 145 patients with central nervous system diseases. Abnormal, especially early components were observed in 32 of 50 patients with multiple sclerosis. Abnormally delayed SEPs were found in 5 of 13 patients with brainstem lesions presenting sensory disorders. The patients with severe cortical parietal lesions (19 cases) or severe thalamic lesions (4 cases) had also severe abnormalities of all components of the SEPs in both P and F regions. A "dissociated" aspect of the SEPs, with absence of early components on the F side and normal components on the P side, occurred in patients with slight thalamic lesions, ataxic hemiparesis or pure motor deficits (prerosublandic lesions). Another dissociated aspect was noted between the normal early SEPs and the abnormal late components in patients with partial parietal lesions, aphasia or in children with acute sclerosing panencephalitis. These "dissociated" aspects of the SEP suggest different, independent afferent pathways, which may be selectively altered. The late components of the SEP may originate from the primary somatosensory cortex and depend on its integrity. Patients with only a pain sensory loss had abnormal late SEP components.
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PMID:Dissociation of parietal and frontal somatosensory evoked potentials in central nervous system diseases. 208 Nov 24

Despite astounding progress in the biochemical management of Parkinson's disease in particular and of other movement disorders, there are still patients disabled by severe tremor and not by bradykinesia in whom thalamotomy remains the treatment of choice. Though the irreducible complications of surgery must be taken into account, the problems of prolonged multiple drug therapy should not be ignored. The same rationale applies to selected patients with essential or familial tremor. For some patients with ataxic tremor caused by multiple sclerosis and other brain lesions, or with dystonia or, rarely, other movement disorders, thalamotomy may offer limited though significant relief from an otherwise intractable disability. Indications for the use of stereotactic destructive lesions in the treatment of nociceptive pain in those cases where cordotomy and intraspinal morphine infusion are unsuitable have contracted with the introduction of lower-risk alternatives such as intraventricular morphine instillation. When destructive lesions are indicated, the choice will lie between mesencephalic tractotomy, with its higher success rate but irreducible mortality and morbidity, and medial thalamotomy, which, though less risky, is also less effective. For central and deafferentation pain, the same two procedures may be considered. However, destructive lesions are seldom effective for the treatment of the most common element of these pain syndromes: steady burning or dysesthetic pain. They may be more promising, though, for the intermittent, often shooting pain and the evoked elements (hyperpathia and allodynia) of central and deafferentation pain. Even so, it is advisable first to carry out a trial of VC and PVG stimulation before considering a destructive lesion, which should be a last resort.
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PMID:Thalamotomy. 213 73

Although pain is not considered a typical symptom of multiple sclerosis, more than 50% of patients with MS present with pain syndromes. In the setting of an incurable disease, symptom control and particularly pain control is very important in achieving a better quality of life. For paroxysmal pain syndromes such as trigeminal neuralgia or painful tonic seizures, carbamazepine and other anticonvulsive drugs are the cornerstone of treatment. On the other hand, drugs are not always effective in treating the various chronic pain syndromes such as dysesthetic extremity pain or leg spasms. In these conditions, individualized regular physiotherapy may relieve pain.
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PMID:[Pain in multiple sclerosis. Clinical aspects and therapy]. 214 31

The trigeminal reflexes (corneal reflex, blink reflex, masseter inhibitory periods, jaw-jerk) and far field scalp potentials (nerve, root, brainstem, subcortical) evoked by percutaneous infraorbital stimulation were recorded in 30 patients with "idiopathic" trigeminal neuralgia (ITN) and 20 with "symptomatic" trigeminal pain (STP): seven postherpetic neuralgia, five multiple sclerosis, four tumour, two vascular malformation, one Tolosa-Hunt syndrome, and one traumatic fracture. All the patients with STP and two of those with ITN had trigeminal reflex abnormalities; 80% of patients with STP and 30% of those with ITN had evoked potential abnormalities. The results indicate that 1) trigeminal reflexes and evoked potentials are both useful in the examination of patients with trigeminal pain, and in cases secondary to specific pathologies provide 100% sensitivity; 2) in "symptomatic" and "idiopathic" paroxysmal pain the primary lesion affects the afferent fibres in the proximal portion of the root or the intrinsic portion in the pons; 3) primary sensory neurons of the A-beta fibre group are involved in both paroxysmal and constant pain, but in the latter the damage is far more severe.
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PMID:Idiopathic and symptomatic trigeminal pain. 229 93

Trigeminal neuralgia is an exactly defined syndrome with a non-uniform aetiology but an obviously uniform pathogenesis. A subdivision in an idiopathic and a symptomatic type is non-essential. In a part of the cases microvascular compression of the sensory root may be the cause of trigeminal neuralgia but there are some good arguments against this concept. Other causes such as multiple sclerosis, acoustic neuroma or carotid aneurysm are well known. The principle of neurosurgical procedures is either an interruption of the pain-conducting fibres or a non-specific manipulation at the Gasserian ganglion or the sensory root with the result of an interruption of abnormal ephapses and short-circuits which may recur later on. So microvascular decompression should not be considered to be a specific and causal therapeutic approach as well as the therapy of first choice for all cases.
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PMID:[Etiology and therapy of trigeminal neuralgia]. 229 39

Baclofen, the most effective drug for treating spasticity, is a specific agonist of gamma-aminobutyric acid-B receptors, and is very abundant in the superficial layers of the spinal cord. Given orally, baclofen does not easily penetrate the blood-brain barrier, and is distributed equally to the brain and spinal cord. Direct intrathecal administration was given in order to change the distribution of the drug by preferentially perfusing the spinal cord. Eighteen patients presenting a severe spastic syndrome were treated with chronic intrathecal infusion of baclofen in the lumbar cerebrospinal fluid. After clinical preselection, 38 patients were implanted with a lumbar access port allowing long-term trials in order to determine the efficacy of baclofen therapy and the effective 12-hour dose. The 18 patients selected for chronic administration were implanted with a programmable pump. The pathology in these cases was: multiple sclerosis (6 cases), posttrauma spastic syndrome (eight cases), and (one case each) cerebral palsy, ischemic cerebral lesion, spinal ischemia, and transverse myelitis. The mean follow-up period was 18 months (range 4 to 43 months). The clinical results were evaluated according to muscular hypertony on Ashworth's scale (changed for occurrence of painful spasms) and functional improvement. Results were better for spastic syndrome secondary to traumatic medullary lesion than for demyelinating disease. Hypertonia was improved in all cases as confirmed by the registration of the Hoffman (H) reflex. Painful muscular spasms disappeared in 14 of the 16 affected patients. Significant functional improvement was noted in nine patients and was considerable in three. The risk of side effects secondary to overdose (such as excessive hypotonia or central depression) and the absence of a specific baclofen antagonist stresses the necessity for accurate determination of the efficient dose. After an initial titration period and adjustment of the therapeutic dose, the individual doses were from 21 to 500 micrograms/24 hrs (mean 160 micrograms/24 hrs). This new conservative method is very effective, perfectly reversible, and safe when administered in conditions favorable to its use.
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PMID:Chronic intrathecal baclofen administration for control of severe spasticity. 230 74

A 56 year-old man presented with vertigo and the right sided weakness. Neurological examination revealed a lethargic man with good orientation to three spheres. His neck was supple. He had anisocoria, the right pupil being larger than the left by 1.5 mm with sluggish light reaction bilaterally. He had exotropia of the right eye in primary gaze. The abduction of both eyes were full with terminal horizontal nystagmus. The adduction of both eyes were quite limited in each eye. He had a limited upward gaze with poor convergence. These were interpreted as the syndrome of the medial longitudinal fasciculus (MLF) bilaterally. He had a depressed gag reflex on the right side with tongue deviation to the right. He had a mild weakness of the right side limb and also had the right sided hemihyperesthesia including his face to pain and temperature. Twenty four hours after the onset, the left brachial angiography revealed a complete occlusion of the rostral portion of the basilar artery without visualization of the posterior cerebral and superior cerebellar arteries bilaterally. CT scans three days after the onset revealed a low density area in the mid pons with extension rostrally up to the mesencephalon. Four days later he became quadriplegic with bilateral horizontal gaze palsy. No more internuclear ophthalmoplegia is noted on both sides. The midline location of the MLF in the pons, and the separate blood supplies by different paramedian branches of the basilar artery, form the anatomical explanation for the frequent unilaterality of vascular and bilaterality of demyelinating lesions. Bilateral MLF syndrome has been considered almost pathognomonic of multiple sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral internuclear ophthalmoplegia in association with basilar artery occlusive disease]. 235 Sep 28

The clinical characteristics and course of acute transverse myelopathy (ATM) was studied. One patient developed multiple sclerosis. In 1 patient ATM was caused by tumour-cell embolization of the intramedullar vessels; 30 aged 12-74 years (median 36 years) had ATM of unknown course, of these, 13 had symptoms of a preceding viral-like infection, 18 had back-pain and 10 signs of spinal shock. The time from onset of ATM to maximum deficit varied from less than 1 h to 20 days. The thoracic region was the most common level of cord damage. Follow-up was possible in 29 cases; 2 died (2 and 8 months after onset), of the surviving 27 (follow-up 1-13 years, median 6 years) one third had a good outcome, one third a fair, while one third remained paraplegic, incontinent with severe sensory deficits. Back-pain and signs of spinal shock indicated a poor outcome.
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PMID:Clinical course and long-term prognosis of acute transverse myelopathy. 237 46

The post-poliomyelitis syndrome (PPS) refers to symptoms of new weakness, fatigue, and pain years after recovery from acute poliomyelitis. Oligoclonal IgG bands have been reported in the cerebrospinal fluid (CSF) from PPS patients, suggesting that the syndrome is immune mediated or caused by persistent viral infection. We studied 15 paired serum and CSF samples and 6 unpaired CSF samples from a total of 21 patients with a prior history of poliomyelitis. Quantitative immune studies failed to show evidence for increased intrathecal IgG production relative to patients with noninflammatory central nervous system (CNS) disease. We found definite oligoclonal IgG bands in the CSF from only 1 patient, who also carried a diagnosis of multiple sclerosis. An isoelectric focusing poliovirus antigen overlay study showed evidence that suggested a CNS-specific antipoliovirus immune response in only 1 patient. Our results fail to support a dysimmune or persistent viral cause for post-poliomyelitis progressive muscular atrophy or PPS.
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PMID:Isoelectric focusing studies of serum and cerebrospinal fluid in patients with antecedent poliomyelitis. 217 20


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